| Project/Area Number |
15K19365
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | University of Tsukuba |
|---|
Principal Investigator |
KIMURA Taizo 筑波大学, 附属病院, 病院講師 (00636508)
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 心筋梗塞 / テネイシンC / マクロファージ / 心室リモデリング / toll like receptor 4 / 心筋梗塞後炎症 |
|---|
| Outline of Final Research Achievements |
Left ventricular remodeling after myocardial infarction (MI), which is major cause of heart failure,is one of the important clinical issues.
In this study, we showed that Tenascin-C (TNC), an extracellular matrix glycoprotein,increased the infiltration of pro-inflammatory macrophages and decreased the infiltration of anti-inflammatory macrophages in infarcted myocardium of mice and aggravated left ventricular remodeling after MI.In vitro analysis, induction of anti-inflammatory macrophages from mouse bone marrow derived cells was significantly suppressed by adding TNC and this effect was inhibited by toll like receptor 4 inhibitor. These findings suggest, TN-C aggravates the left ventricular remodeling after MI partly through the promotion of inflammatory response via the regulation of macrophage subsets.
TNC might be a new biotarget to prevent adverse ventricular remodeling after MI.
|
